Myocardial infarction is the guiding cause of high mortality in all cardiovascular diseases [
32]. Mortality after myocardial infarction has decreased essentially over the past few decades, while there is still important in-hospital mortality [
33]. Therefore, research on the pathogenesis and treatment mechanism of AMI has become a top priority. Many biologists and medical researchers have invested in the pathogenesis of AMI. They mainly focused on some certain genes, and some researches had achieved results in proteins and related signal transductions. A series of analytical methods was combined to explore the pathogenesis of AMI. The complete expression profile of AMI disease samples was constructed for DEGs analysis, and 4551 potential pathogenic genes were screened. The increased SCD content indicated that SCD may be the key gene for AMI. The results of the study suggested that the ischemic time from the onset of symptoms to coronary reperfusion appears to be the strongest factor affecting thrombus in myocardial infarction [
34]. Co-expression analysis of the DEGs revealed that we obtained 7 co-expression modules, and the genes contained in the modules were considered to have synergistic expression. Based on the results of the functional enrichment analysis, it was found that 7 modules were mainly involved in response to reactive oxygen species. According to studies by many scholars, N-acetylcysteine (NAC) is an antioxidant with active oxygen scavenging properties, which has the effect of enhancing nitroglycerin [
35]. The enrichment of pathways revealed that functional block genes were primarily involved in the AMPK signal transduction, which might trigger AMI. This suggested that the AMPK signaling cascade was thought to be the core signal transduction that triggered AMI. Yang et al. [
36] accentuated the AMPK signal transduction has key functions in intracellular adaptation to energy stress during myocardial ischemia. Inhibition of AMPK signaling by Notch1 enhances cardiac dysfunction caused by myocardial infarction [
36]. The TFs which were involved in these 7 dysfunction modules, were obtained, and there were 26 Pivot-Module interaction pairs. NFκB1 regulated 2 dysfunction modules, thereby promoting the occurrence and development of AMI. According to Boccardi et al. [
37], it was found that NFκB was involved in various human diseases, including atherosclerosis and myocardial infarction. Studies had shown that the -94 ins/del ATTG NFκB1 gene variant might lead to a decrease in myocardial infarction sensitivity by a potential reduction in activation of NFκB, which in turn was associated with a decrease in plasma inflammatory markers [
37]. Both MECP2 and SIRT1 had regulatory functions in 1 functional module and occupied an indispensable position in the potential pathogenesis of AMI. On the one hand, the anti-apoptotic effect of miR-22 was to protect myocardial infarction by targeting MECP2 [
38] directly. On the other hand, SIRT1 was known to be a nicotinamide adenine dinucleotide-dependent histone deacetylase, which makes the heart more resistant to ischemic injury. SIRT1 may be a new promising therapeutic target for myocardial infarction [
39]. The expression of SIRT1 was down-regulated by many stress stimuli in the heart. These stimuli might jointly drive the pathogenesis of AMI [
40]. Moreover, ncRNA had been recognized as an important regulator in the development and progression of the disease. In this regard, a pivot analysis was performed, based on the targeting relationship between ncRNA and genes. The predicted results showed that 782 ncRNA had important regulatory effects on the modules, involving 1239 ncRNA-Module interaction pairs. These ncRNAs affected the development of AMI in varying degrees. The results of statistical analysis revealed that miR-519d-3p had important regulatory functions in 6 dysfunction modules, which might affect the progression of AMI. Down-regulation of miR-519d-3p and over expression of HOX transcript antisense RNA(HOTAIR) had been reported reducing myocardial apoptosis induced by myocardial infarction or hypoxia. It can provide a potential therapeutic target for myocardial infarction [
41]. Both TUG1 and miR-93-5p had essential regulatory relationships with the 4 dysfunction modules, and had important functions in module dysfunction. On the one hand, TUG1 can inhibit apoptosis in hypoxia-induced injury of H9c2 cell, thereby reducing hypoxia-induced cell damage and inhibiting myocardial infarction [
42]. On the other hand, the data showed that the expression of miR-93-5p had a cardioprotective effect in AMI. The Adipose-derived stromal cells (ADSCs)-derived exosomes enhanced by miR-93-5p could prevent cardiac damage by inhibiting autophagy and inflammatory responses [
43]. The series of regulatory factors predicted by this study had a certain degree of regulation on the pathogenesis of AMI.
Actually, there are many other mechanisms underlying AMI. Adiponectin and insulin resistance play a critical role in progression of any stage of ischemic heart disease [
44]. Tight glycemic control may improve outcome of ST-segment elevation myocardial infarction and increase regenerative potential of the ischemic myocardium after acute myocardial infarction [
45,
46]. The potential interplay between subclinical hypothyroidism and inflammatory activity makes atherosclerotic plaque progression toward instability, resulting in the innate immunity-dependent plaque rupture [
47]. Ubiquitin–proteasome deregulation is proposed as the pathogenic factor mediating the progression of the plaque [
48] and Myocardial carbonic anhydrases activation is associated with ischemic cardiomyopathy in diabetic patients [
49]. However, except for the key factors which are above-mentioned, other unmentioned factors might have functions in the mechanism of dysregulation of AMI, which need to be further explored.